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Clin Med II Infectious Disease Lecture II—Viral Diseases, part 2/3.

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Presentation on theme: "Clin Med II Infectious Disease Lecture II—Viral Diseases, part 2/3."— Presentation transcript:

1 Clin Med II Infectious Disease Lecture II—Viral Diseases, part 2/3

2 Herpes Simplex Virus

3 What’s with all the numbers? Human Herpesviruses  HHV 1—Herpes Simplex Virus type 1  HHV 2—Herpes Simplex Virus type 2  HHV 3—Varicella Zoster Virus  HHV 4—Epstein-Barr Virus  HHV 5—Cytomegalovirus  HHV 6—Roseola Infantum  HHV 7—”The Multitasker”  Roseola, Seizures, Encephalitis, “helps” CMV in renal transplants  HHV 8—Kaposi sarcoma/primary effusion lymphoma

4 Herpes Simplex Virus  HSV-1—oral  HSV-2—genital  Risks—in text—black race, female gender, lower socioeconomic status, and high-risk sexual history  Asymptomatic shedding  HSV-2 and HIV—linked  HSV-2 increases risk of HIV HSV-2 reactivates more often in advanced HIV  HSV-2 suppression can decrease HIV-1 plasma level and genital tract shedding

5 Mucocutaneous HSV-1  HSV-1—mouth and oral cavity  ”herpes labialis” or “gingivostomatitis”  Herpetic whitlow—painful digital lesions  Herpes gladiatorum—painful rash transmitted classically by sports contact  Frequent asymptomatic shedding—monthly or more  Vesicles  ulcers (1-2 days)  epithelialization (1-2 wks)  Recurrences--fewer lesions, labial, heal faster  Triggers—stress, fever, infection, sunlight, chemo, ???

6 Mucocutaneous HSV-1

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9 Mucocutaneous HSV-2  Primarily involves genital tract  May affect perianal region, buttocks, upper thighs  Multiple, painful, small, grouped, vesicular lesions  Dysuria, cervicitis, urinary retention  Increased HSV-2 lesion rates—postpartum period and among women who have sex with women  HIV patients—proctitis and sacral lesions  extensive, ulcerating, weeping lesions  Drug-resistant isolates—large ulcerations, atypical lesions

10 Mucocutaneous HSV-2

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13 Mucocutaneous HSV Diagnosis  Clinical  Standard—viral cultures of vesicular fluid or direct immunofluorescent antibody staining of lesions  Intranuclear inclusion bodies  Multinucleated giant cells on Tzanck smear or Calcofluor prep

14 Mucocutaneous HSV  Treatment often not necessary in immunocompetent pts  Genital infection—oral agents—acyclovir, valacycloivr, famiciclovir  Primary—7-10 days and higher doses; Recurrent—1-3 days  Primary herpes labialis—oral antivirals as for primary genital  Recurrent herpes labialis—topical acyclovir and hyrocortisone, topical penciclovir, or oral antivirals  Immunocompromised—consider IV antivirals  Atypical isolates, large ulcerations, new lesions, poor response  Secondary prophylaxis—recurrent infections—daily oral antivirals

15 Ocular HSV  Keratitis, Blepharitis, Keratoconjuncitvits  If epithelial—heal without vision impairment  If stroma involved— uveitis, scarring, blindness  Frequent recurrence  Second most common cause of acute retinal necrosis

16 Ocular HSV  Branching (dendritic) ulcers on fluorescein stain  Treat with topical antivirals  Acute retinal necrosis—IV acyclovir or oral famciclovir  Topical steroids—may exacerbate  Long term treatment can reduce recurrences

17 Congenital/Neonatal HSV  HSV-1 and HSV-2  Congenital—organomegaly, bleeding, CNS abnormalities  Neonatal is more common than congenital  Highest risk—maternal infection in 3 rd trimester  70% of infections are asymptomatic or unrecognized

18 Congenital/Neonatal HSV  Treat disseminated lesions with IV acyclovir for 2-3 weeks  Counseling with serologic screening should be offered to pregnant mothers  Maternal antenatal suppressive therapy with acyclovir at 36 weeks gestation  C-section for pregnant women with active genital lesions or prodromal symptoms

19 HSV and CNS Disease  HSV-1: HSV Encephalitis, may enhance Alzheimer disease  Encephalitis symptoms: flu-like prodrome, headache, fever, behavioral or speech disturbances, seizures  High mortality rate—untreated, presentation with coma  Does not occur disproportionately among immunocompromised  HSV-2: Meningitis (primary or recurrent)  Both HSV-1 and HSV-2: benign recurrent lymphocytic meningitis; mild, nonspecific neurologic symptoms

20 HSV Encephalitis and Recurrent Meningitis  CSF Pleocytosis common  HSV DNA PCR of CSF— rapid, sensitive, specific but can have up to 25% false negatives  MRI scanning—increased signal in temporal and frontal lobes  IV acyclovir q 8 hours for 10+ days if suspected HSV encephalitis  Long term neurologic sequelae are common

21 HSV Encephalitis

22 Other HSV Manifestations  Disseminated—immunosuppression, pregnancy  Bell’s Palsy—associated with HSV-1  Esophagitis—HSV-1; immunocompromised  Proctitis—primarily in men who have sex with men  Erythema multiforme—leading association with EM and SJS (along with medications)  Acute liver failure—1% of cases but 75% mortality  Lower respiratory tract—mechanically ventilated pts  HSV-1—perinephric abscess, febrile neutropenia, chronic urticaria, SLE-related esophagitis and enteritis, H. pylori- negative upper GI ulcers, atrial myxoma

23 HSV Prevention  Antiviral suppressive therapy  Counseling  Barrier precautions  Disclosure of partner status—50% decrease in HSV-2 transmission  Hand washing and glove/gown precautions  HSV-2 glycoprotein D vaccine is under development

24 Varicella Zoster Virus

25  Manifests as chickenpox (varicella) and shingles (zoster)  Varicella—typically in childhood; incubates days  Highly contagious— droplet inhalation or lesion contact  Zoster—up to 25% of population; increases with age

26 Varicella  Fever and malaise  Pruritic rash  Maculopapules  vesicles  pustules  crusts  Multiple stages of eruption usually present simultaneously  “dew drop on rose petal”  Complications—secondary bacterial infection, pneumonitis, encephalitis—in 1%  More severe in older pts and immunocompromised

27 Zoster  Mostly among adults  Pain—severe—often precedes rash  Varicella-like lesions—usually in dermatomal distribution  Herpes Zoster Ophthalmicus—lesions on tip of nose, inner corner of eye, and root and side of the nose (Hutchinson sign)  Herpes Zoster Oticus—facial palsy, lesions of ear +/- TM involvement, vertigo, tinnitus, deafness (Ramsay Hunt syndrome)  Contact with varicella patients—not a risk factor

28 Herpes Zoster Ophthalmicus

29 Herpes Zoster Oticus

30 Varicella Zoster Virus  Diagnosis—usually clinical  Confirm with direct immunofluorescent antibody staining or PCR of scrapings from lesions  Multinucleated giant cells on Tzanck smear  Leukopenia and subclinical AST/ALT elevation  Thrombocytopenia  Varicella skin test and ELISPOT—VZV susceptibility

31 Varicella Complications  Secondary bacterial skin superinfections  Interstital VZV pneumonia  Neuro—cerebellar ataxia, encephalitis  Purpura fulminans—extremely rare  Liver—hepatitis, Reye’s syndrome  Pregnancy—  1 st or 2 nd trimesters, small risk of congenital malformations  3 rd trimester, risk of disseminated disease

32 Zoster Complications  Postherpetic neuralgia—60-70% of pts >60 years old  Bacterial skin superinfections  Herpes zoster ophthalmicus or unilateral ophthalmoplegia  Cranial nerve involvement  Aseptic meningitis  Peripheral motor neuropathy  Transverse myelitis  Encephalitis  Acute cerebellitis  Stroke or vasculopathy  Acute retinal necrosis or progressive outer retinal necrosis

33 VZV Encephalitis

34 VZV—Treatment  General treatment measures—initial isolation; bed rest till afebrile; control of pruritis  Antivirals—Acyclovir within 24 hours after rash onset  Consider—patients over 12 years old, secondary contacts, patients with chronic cutaneous and cardiopulmonary disease, and children on long-term salicylate therapy  High dose IV antivirals—for immunocompromised patients, pregnancy (3 rd trimester), extracutaneous disease  Prophylaxis for profoundly immunosuppresed patients  Postherpetic neuralgia—gabapentin, lidocaine patches  Tricyclic antidepressants, opioids, capsaicin cream  Epidural injection of steroids and anesthetics

35 VZV—Prognosis and Prevention  Varicella—duration usually 2 weeks or less; fatalites rare  Zoster—2-6 weeks; greater antibody response  Ophthalmic involvement—periodic exams  Screen healthcare workers and vaccinate if negative  Workers with zoster should receive antiviral agents during 1 st 72 hours of disease and stay away from work until lesions are crusted  Isolate patients with active VZV from negative contacts

36 Varicella Vaccination  Universal childhood vaccination against varicella—98.1% effective when given after 13 months of age  1 st dose months, 2 nd dose 4-6 years  Avoid aspirin for at least 6 weeks  Seronegative individuals over 13 years old—2 doses of varicella vaccine 4-8 weeks apart  Consider vaccination for HIV + adolescents and adults with CD4 200 cells/mcL or higher  Also other selected immunocompromised pts (see text)  Varicella incidence decreased 67%-87% due to vaccination  Postexposure vaccination recommended for unvaccinated persons without other evidence of immunity  Varicella Zoster immunoglobulin—consider for susceptible pts who cannot receive vaccine

37 Zoster Vaccination  Live attenuated VZV vaccine—for patients 60 and older  Reduces incidence of postherpetic neuralgia by 67%  Reduces incidence of herpes zoster by 51%  Should not co-administer with pneumonia vaccine

38 Rabies

39  Viral encephalitis transmitted by infected saliva  50, ,000 deaths/year globally  In US—dog rabies has almost disappeared, but wildlife rabies has greatly increased  Incubation—10 days to years (usually 3-7 weeks)  Inoculation site  nerves  brain  efferent nerves  salivary glands  Forms cytoplasmic inclusion bodies  Almost uniformly fatal

40 Rabies Symptoms  History of animal bite (may not notice bat bite)  Pain (at bite location), fever, malaise, headache, nausea, vomiting  Aerophobia and sensitivity to temperature change  Percussion myoedema  10 days after prodrome—CNS stage  Encephalitic—”furious”—80%--classic rabies symptoms  Paralytic—”dumb”—20%--acute ascending paralysis  Progresses to coma, ANS dysfunction, and death

41 Rabies Diagnosis  Bitten animals that appear well—quarantine 10 days  Ill or dead animals—test for rabies  If animal cannot be examined—presume that raccoons, skunks, bats, foxes, bats and foxes are rabid  Direct fluoroscent antibody testing—skin material from posterior neck—60-80% sensitivity  Definitive diagnostic assays—  RT-PCR  nucleic acid sequence-based amplification  direct rapid immunohistochemical test  viral isolation from CSF or saliva

42 Rabies Treatment  Intensive care—airway, oxygenation, seizure control  Universal precautions  Postexposure prophlaxis given prior to symptoms—nearly 100% successful in disease prevention  Once symptoms have appeared, death almost inevitably occurs after 7 days, usually from respiratory failure

43 Rabies—Prevention  Immunization of household dogs, cats, and patients with significant animal exposure  Cleansing, debridement, and flushing of wounds  Do not suture animal bite wounds  Decision to treat with immune globulin or antiserum— varies with circumstances of bite  Consult with state and local health departments  Give treatment as promptly as possible if indicated  Read—when to admit, when to refer

44 Questions?


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